Peyer's patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion.
Peyer's patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion.
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DOI：
10.1084/jem.20181210
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发表时间：
2018-11-05
期刊：
影响因子：
--
通讯作者：
Lecuit M
中科院分区：
文献类型：
--
作者：
Disson O;Blériot C;Jacob JM;Serafini N;Dulauroy S;Jouvion G;Fevre C;Gessain G;Thouvenot P;Eberl G;Di Santo JP;Peduto L;Lecuit M
单核细胞增生李斯特菌（Listeria monocytogenes，Lm）通过杯状细胞（GCs）穿过肠绒毛屏障。Disson等人表明，淋巴集结骨髓细胞的Lm感染向绒毛基质细胞发出信号，导致表达管腔可及E-钙粘蛋白的GC减少，从而阻断绒毛感染，同时有利于结肠炎。食源性病原体单核细胞增生李斯特菌（Lm）在Lm表面蛋白InlA与其受体E-钙粘蛋白相互作用后，通过杯状细胞（GC）穿过肠绒毛上皮。在这里，我们表明，Lm感染加速肠绒毛上皮细胞的更新，同时减少了GC的数量表达管腔可及的E-钙粘蛋白，从而锁定Lm的入口。这种针对肠道病原体的新型先天性免疫应答是由派伊尔斑CX 3CR 1+细胞的感染和随后的IL-23产生触发的。它需要上皮细胞中的STAT 3磷酸化以响应固有层gp 38+基质细胞表达的IL-22和IL-11。Lm诱导的上皮细胞中的IFN-γ信号传导和STAT 1磷酸化对于Lm相关的肠上皮反应也是至关重要的。GC消耗还导致结肠粘液屏障厚度的降低，从而增加宿主对结肠炎的易感性。这项研究揭示了一种新的先天性免疫反应的肠道病原体，其中涉及gp 38+基质细胞和锁定肠绒毛入侵，但有利于结肠炎。
Listeria monocytogenes (Lm) crosses the intestinal villus barrier via goblet cells (GCs). Disson et al. show that Lm infection of Peyer’s patch myeloid cells signals to villus stromal cells, leading to a decrease of GCs expressing luminally accessible E-cadherin, thereby blocking villus infection while favoring colitis. The foodborne pathogen Listeria monocytogenes (Lm) crosses the intestinal villus epithelium via goblet cells (GCs) upon the interaction of Lm surface protein InlA with its receptor E-cadherin. Here, we show that Lm infection accelerates intestinal villus epithelium renewal while decreasing the number of GCs expressing luminally accessible E-cadherin, thereby locking Lm portal of entry. This novel innate immune response to an enteropathogen is triggered by the infection of Peyer’s patch CX3CR1+ cells and the ensuing production of IL-23. It requires STAT3 phosphorylation in epithelial cells in response to IL-22 and IL-11 expressed by lamina propria gp38+ stromal cells. Lm-induced IFN-γ signaling and STAT1 phosphorylation in epithelial cells is also critical for Lm-associated intestinal epithelium response. GC depletion also leads to a decrease in colon mucus barrier thickness, thereby increasing host susceptibility to colitis. This study unveils a novel innate immune response to an enteropathogen, which implicates gp38+ stromal cells and locks intestinal villus invasion, but favors colitis.
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影响因子：
56.3
作者：
Charlier, Caroline;Perrodeau, Elodie;Lecuit, Marc
通讯作者：
Lecuit, Marc
影响因子：
64.8
作者：
Cuylen S;Blaukopf C;Politi AZ;Müller-Reichert T;Neumann B;Poser I;Ellenberg J;Hyman AA;Gerlich DW
通讯作者：
Gerlich DW
影响因子：
64.8
作者：
通讯作者：
--
影响因子：
48
作者：
de Chaumont, Fabrice;Dallongeville, Stephane;Olivo-Marin, Jean-Christophe
通讯作者：
Olivo-Marin, Jean-Christophe
影响因子：
64.5
作者：
Chudnovskiy, Aleksey;Mortha, Arthur;Kana, Veronika;Kennard, Andrea;Ramirez, Juan David;Rahman, Adeeb;Remark, Romain;Mogno, Ilaria;Ng, Ruby;Gnjatic, Sasha;Amir, El-ad David;Solovyov, Alexander;Greenbaum, Benjamin;Clemente, Jose;Faith, Jeremiah;Belkaid, Yasmine;Grigg, Michael E.;Merad, Miriam
通讯作者：
Merad, Miriam